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1.
目的研究氟化钠(NaF)对大鼠肾脏脂质过氧化作用的影响及亚硒酸钠(Na2SeO3)对氟肾脏毒性的保护作用。方法大鼠经饮水加入NaF(15mmol/L)或/和Na2SeO3(15μmol/L)染毒120天,观察氟在机体的蓄积、排泄,尿酶活性及肾脏脂质过氧化水平的变化。结果氟染毒后,大鼠血氟水平、尿氟水平、骨氟含量,尿谷氨酰转肽酶(γGT)、N乙酰βD氨基葡萄糖苷酶(NAG)、琥珀酸脱氢酶(SDH)活性及肾脏活性氧自由基(OFRS)相对浓度、脂质过氧化降解产物丙二醛(MDA)含量均显著升高,谷胱甘肽过氧化物酶(GSHPx)活性及GSH含量显著下降。同时补加亚硒酸钠,可促进尿氟排泄,降低血氟水平及骨氟含量,降低尿酶γGT、NAG、SDH活性和肾脏OFRS、MDA含量,同时提高肾脏GSHPx活性,但对GSH含量影响不显著。结论氟化钠引起肾脏损伤与其诱导脂质过氧化作用增强有关,亚硒酸钠对氟化钠致肾脏毒性具有拮抗作用。 相似文献
2.
缺锌对大鼠脂质过氧化及抗氧化系统的影响 总被引:14,自引:0,他引:14
研究缺锌对3周龄大鼠的脂质过氧化和抗氧化系统的影响。方法:健康Wistar大鼠33只,雌雄各半,按体重随机分为A(缺锌组),B(自由进食对照组),C(配对喂养组)。每组11只,实验期40天。观察指标有血清和肝脏锌,肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性,血清和肝脏丙二醛(MDA),并采用电子自旋共振(electronspinresonance,ESR)及自旋捕捉技术直接测定大鼠肝组织中的氧自由基。结果:A组大鼠肝脏SOD、GSH-Px活性明显下降,血清和肝脏MDA含量显著升高,ESR图谱出现了N-H偶合的三组双峰波。结论:缺锌可以使大鼠脂质过氧化反应明显加强,而抗氧化能力明显减弱。 相似文献
3.
探讨了给予二甲基亚硝胺(NDMN),同时补充β-胡萝卜素(β-C)后,大鼠体内抗氧化酶活性和脂质过氧化物含量的变化。结果显示,一定剂量的NDMN可使大鼠血红细胞、肝肾匀浆SOD活性和全血GSH-Px活性下降(P<0.05),血清和肝MDA和血清ROOH产生增多(P<0.05)。添加β-C(25mg/kg)后,SOD和GSH-Px活性均比单纯NDMN组有明显提高(P<0.05)。MDA和ROOH含量明显低于NDMN组(P<0.05)。提示自由基和脂质过氧化反应可能也是NDMN及其它亚硝胺致癌的途径之一;一定剂量的β-C可对抗NDMN引起的自由基和脂质过氧化。 相似文献
4.
β-胡萝卜素和核黄素对大鼠脂质过氧化的影响 总被引:12,自引:1,他引:11
目的:进一步探讨亚硝胺通过脂质过氧化而致癌的可能途径,以及研究β-胡萝卜素(β-C)和核黄素(VB2)通过抑制脂质过氧化反应而影响亚硝胺致癌的可能途径。方法:将50只二级SD雄性大鼠随机分成5组。实验组在每日灌胃二甲基亚硝胺(NDMN)1.75mg/kg的基础上,每日分别给予β-C25mg/kg和/或VB218mg/kg补充,实验期为28天。实验结束时,收集血液,摘取肝脏和肾脏,测红细胞和肝肾匀浆SOD活性,全血GSH-Px活性,血清和肝肾匀浆MDA含量,血清ROOH以及全血Hb含量。结果:1.NDMN可使SOD和GSH-Px活性下降(P<0.05),MDA和ROOH产生增多(P<0.05)。2.添加β-C后,SOD和GSH-Px活性有明显提高(P<0.05),MDA和ROOH的含量明显降低(P<0.05)。3.添加VB2后,肝SOD和全血GSH-Px活性均有明显提高(P<0.05),但MDA和ROOH的含量没有差异(P>0.05)。4.同时补充β-C和VB2后,各项指标的变化与单纯β-C组基本一致。结论:脂质过氧化也是亚硝胺致癌的途径之一;一定剂量的β-C可对抗NDMN引发的脂质过氧化;核黄素对提高抗氧化? 相似文献
5.
硒、维生素E对心肌胶原蛋白代谢的影响 总被引:5,自引:1,他引:4
目的:阐明硒(Se)、维生素E(VE)与心肌胶原蛋白代谢的关系。方法:以病区粮(低Se、低VE)喂养大鼠,并注射异丙基肾上腺素(ISO)诱发心肌缺血缺氧性坏死,检测心肌中谷胱甘肽氧化酶(GSH-PX)、过氧化氢酶(CAT)、丙二醛(MDA)和胶原蛋白含量变化。结果:低Se低VE组血浆和心肌GSH-PX、CAT活性下降,MDA含量上升,与心肌胶原蛋白含量变化有相关性。补Se补VE后,GSH-PX、CAT活性上升,MDA水平下降,心肌胶原蛋白含量下降。结论:低Se低VE加重ISO诱发的心肌损伤,脂质过氧化和自由基与心肌胶原蛋白代谢关系密切。补Se补VE后,能缓解心肌细胞对诱发因素所造成的损伤,对保护心肌细胞和防止心肌纤维化的形成具有一定作用。 相似文献
6.
硒强化沙棘果汁对大鼠机体脂质过氧化作用的影响 总被引:3,自引:0,他引:3
成年Wistar大鼠用含硒强化沙棘果汁、沙棘果汁及维生素C的半纯化饲料喂养12周后,测定其血清、肝脏和红细胞膜丙二醛(MDA)含量,全血及肝脏谷胱甘肽过氧化物酶(GSH-Px)活性及全血超氧化物岐化酶(SOD)活性的变化。结果表明:大鼠血清、肝脏及红细胞膜MDA含量在各实验组均远远低于对照组(P<0.01)。而各实验组GSH-Px和SOD活性均显著高于对照组。结果说明,沙棘果汁可显著降低大鼠机体内脂质过氧化反应,增强机体抵抗过氧化损伤的能力,这种作用在经硒强化后尤为显著。 相似文献
7.
矽肺与NO、氧化及脂质过氧化关系的探讨 总被引:13,自引:2,他引:11
目的探讨矽肺与NO及氧化和脂质过氧化的关系。方法检测73例矽肺患者和60例健康对照者的血浆NO、VitC、VitE、β胡萝卜素(βCAR)、过氧化脂质(LPO)含量及红细胞超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSHPx)活力和LPO含量。结果与对照组比较,矽肺组的血浆VitC、VitE、βCAR含量及红细胞SOD、CAT、GSHPx活力显著降低,血浆NO、LPO含量及红细胞LPO含量显著升高(P<0.05或P<0.01);各检测值与病程均有相关;血浆NO、VitE含量及红细胞SOD活力、LPO含量与病程相关最密切。结论矽肺患者体内的NO代谢异常,氧化和脂质过氧化反应病理性加剧。 相似文献
8.
苦荞蛋白复合物的营养成分及其抗衰老作用的研究 总被引:40,自引:2,他引:40
分析苦荞蛋白复合物的营养成分,观察其抗衰老效果。方法:用碱抽提和等电点沉淀法从苦荞麦籽粒中制备出苦荞蛋白复合物(TBPC),再用含20%TBPC饲料喂小鼠,观察对小鼠血液和脏器中超氧化物岐化酶(SOD)、过氧化氢酶(CAT)和谷胱苷肽过氧化物酶(GSH-Px)的活性的影响。结果:TBPC的蛋白质含量为63.4%,脂肪12.7%,碳水化物10.2%,灰分3.5%,粗纤维0.4%,水分9.8%。用TBPC饲喂后,小鼠血液、肝脏和心脏中SOD、CAT和GSH-Px活性均有不同程度提高,脂质过氧化产物丙二醛(MDA)含量下降。结论:苦荞蛋白复合物对生物体有一定营养和抗衰老作用。 相似文献
9.
绿茶及混合茶抑制二乙基亚硝胺诱发大鼠肝癌前期病变的抗氧化机理研究 总被引:10,自引:1,他引:9
用二乙基亚硝胺(DEN)诱发Wistar大鼠肝癌前期病变(Solt-Farber模型)。实验前6周给大鼠饮用2%绿茶水及0.5%混合茶水,于实验第8周末宰杀动物。结果发现,绿茶组及混合茶组肝r-GT异常病灶数均明显低于阳性对照组(P<0.01)。经HPLC法分离肝微粒体脂质过氧化产物丙二醛(MDA)、乙醛(ACT)、戊醛(PP)、丙酮(ACON),与阳性对照组相比,绿茶组和混合茶组的各种脂质过氧化产物均有不同程度的降低。此外,对多种抗氧化酶和Ⅱ相代谢酶活性进行检测,其中绿茶组SOD、GST、QR活性明显高于阳性对照组;混合茶组CAT、SOD、GST、QR活性明显高于阳性对照组。结果表明,绿茶和混合茶对DEN诱发大鼠肝癌的发生均有显著的预防作用。其作用机理可能和诱导抗氧化酶及某些Ⅱ相代谢酶活性,以及抑制脂质过氧化作用有关。 相似文献
10.
微量元素硒对动脉粥样硬化家兔内皮素的影响 总被引:7,自引:1,他引:7
用放免分析方法,对服Se的动脉粥样硬化(AS)家兔血浆内皮素(ET)水平进行测定。结果表明,Se组家兔血浆ET水平明显低于对照组,同时血清胆固醇(Ch)、低密度脂蛋白(LDL)及过氧化脂质(LPO)含量降低,高密度脂蛋白(HDL)明显增高,全血谷胱甘肽过氧化物酶(GSH-Px)和血清超氧化物歧化酶(SOD)活力也明显提高。提示,Se可通过抗氧化作用保护内皮细胞免遭过氧化损伤,减少ET释放,抑制AS形成和发展。 相似文献
11.
硒对镉在大鼠肝脏亚细胞分布及脂质过氧化作用的影响 总被引:7,自引:3,他引:4
采用给大鼠腹腔注射镉(CdCl_2 1mg/kg)或/和硒(Na_2SeO_3 0.4mg/kg)的方法,研究了硒对镉在大鼠肝脏亚细胞分布及脂质过氧化作用的影响。结果表明,给大鼠连续腹腔注射CdCl_2(1mg/kg)3d,可致大鼠肝微粒体和线粒体脂质过氧化物(LPO)含量显著增加,谷胱甘肽过氧化物酶(GSH-Px)活性显著下降,肝细胞浆还原型谷胱甘肽(GSH)含量显著降低。同时给大鼠腹腔注射Na_2SeO_3(0.4mg/kg),硒可拮抗上述镉的效应。但硒对大鼠肝脏镉含量及镉在肝脏亚细胞分布没有明显影响。 相似文献
12.
Dorval J Leblond V Deblois C Hontela A 《Environmental toxicology and chemistry / SETAC》2005,24(5):1273-1280
The effects of agricultural chemicals on cortisol secretion, antioxidants, and lipid peroxidation were investigated in hepatic and adrenal tissue of white sucker (Catostomus commersoni) from a river (Yamaska) that drains an agricultural region in Québec (Canada). Plasma cholinesterase (ChE) activity, used as a biomarker of exposure to pesticides, was elevated in fish from the reference site compared to fish from the contaminated sites. Plasma concentrations of cortisol and thyroid hormones (T3 and T4) were higher in fish from the reference site compared to contaminated sites; reduced glutathione (GSH) levels, catalase (CAT), and glutathione peroxidase (GPx) activities were higher and lipid peroxidation (LPO) was lower. Levels of antioxidants (CAT, Gpx, and GSH) were higher (10-90%) and LPO levels were lower (50%) in the liver than in the adrenal tissue. The present in situ study provided evidence that antioxidants, lipid peroxidation, and plasma hormones were altered in fish sampled in areas impacted by agricultural chemicals. Endocrine-disrupting effects were associated with oxidative stress. The results suggest that antioxidants and lipid peroxidation could be used as markers of contaminant exposure in fish. 相似文献
13.
Mohammad Q. Hassan Sidney J. Stohs Wallace J. Murray 《Archives of environmental contamination and toxicology》1985,14(4):437-442
The effects of vitamins A and E on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced lipid peroxidation in the rat were investigated. Vitamin E markedly inhibited microsomal lipid peroxidation (malondialdehyde formation), but had no effect on glutathione peroxidase activity or glutathione (GSH) content, and did not protect against decreased body and liver weights. Furthermore, vitamin E had little effect on TCDD-induced lethality in rats. Vitamin A inhibited lipid peroxidation, elevated the activity of glutathine peroxidase and prevented a TCDD-induced decrease in GSH content in the liver. However, vitamin A did not inhibit the decrease in liver and body weights and provided little protection against TCDD-induced lethality. The activities of aryl hydrocarbon hydroxylase, glutathione-S-transferase (GST) and glutathione reductase (GR) increased after treatment with these two vitamins. Administration of vitamins E and A do not provide significant longterm protection against TCDD-induced lethality although they can prevent TCDD-induced microsomal lipid peroxidation as determined by the thiobarbituric acid assay method. 相似文献
14.
[目的 ]探讨电刺激应激对实验动物体内脂质过氧化水平以及抗氧化能力的影响。 [方法 ]采用 5 0Hz的强脉冲、电压为 10 0V交流电对实验大鼠连续 10d进行电刺激 ,观察受刺激后大鼠肝、大脑组织中抗氧化酶GSH Px、GST和抗氧化物质GSH以及反映脂质过氧化水平的脂质过氧化代谢产物MDA的含量。 [结果 ]受试大鼠肝和大脑组织中抗氧化物质GSH含量明显下降和MDA含量明显升高 ,抗氧化酶GSH Px、GST的活性明显下降 ,与对照组相比P <0 0 5和P <0 0 1。 [结论 ]电刺激应激能增强大鼠脑和肝组织脂质过氧化水平 相似文献
15.
亚砷酸钠对大鼠肝线粒体和微粒体酶的影响 总被引:2,自引:0,他引:2
研究了亚砷酸钠在体内、体外对大鼠肝线粒体丙酮酸脱氢酶(PDH)、琥珀酸脱氢酶(SDH)和微粒体酶细胞色素P-450、b5、NAD(P)H-细胞色素C还原酶、谷胱甘肽硫转移酶(GST)的影响;并通过观测亚砷酸钠与亚硒酸钠的作用及其对肝谷胱甘肽过氧化物酶、谷胱甘肽含量和线粒体脂质过氧化的影响,探讨亚砷酸钠的作用机理。结果表明:连续7天腹腔注射20mg/kg的亚砷酸钠,线粒体PDH、SDH被抑制,分别相当于对照组的51%和58%。而亚硒酸钠可有效拮抗砷对PDH、SDH的抑制作用。亚砷酸钠显著降低肝GSH的含量,并增强线粒体膜脂质过氧化作用(P<0.05)。在体内试验中,亚砷酸钠对谷胱甘肽过氧化物酶和肝微粒体酶无明显影响。亚砷酸钠在体外实验中,浓度在10-7~10-3mol/L的范围内,抑制SDH的活力,提高GSH的含量,且呈剂量-效应关系。结果提示,亚砷酸钠对机体的作用与其对LPO和体内巯基的影响有关 相似文献
16.
The purpose of this study was to examine the effect of low, adequate, and high dietary iron (Fe) levels on lipid peroxidation, glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) activities, and glutathione (GSH) concentrations in colon and liver. Male Sprague Dawley rats were fed iron deficient (DFe; 14 mg Fe/kg diet; N=8), adequate iron (AFe; 39 mg Fe/kg diet, N=8), or high iron (HFe; 454 mg Fe/kg diet; N=8) diets for 3 weeks. Liver Fe concentrations were 26, 84, and 243 ug/g wet weight, respectively, for rats fed DFe, AFe, and HFe diets (p<0.0001). Lipid peroxidation was increased 70% in distal colonic mucosa of rats fed HFe diets compared to that of rats fed AFe and DFe diets (p<0.01), but lipid peroxidation was unaffected by diet in proximal colon or liver. While distal colonic mucosal GSH-Px activity was lower in DFe rats (0.062 U/mg protein), than in AFe rats (0.091 U/mg protein), and HFe rats (0.089 U/mg protein) (p<0.05), iron intake had no effect on GSH-Px activity in proximal colon or liver. The distal colon had higher GSH-Px activity than proximal colon (p<0.0001). GST activity in colon and liver, and hepatic GSH concentrations were not altered by dietary iron intakes. This study suggests that distal and proximal colonic mucosa may respond differently to changes in Fe status. 相似文献
17.
扇贝提取物对肝损伤小鼠抗氧化功能的影响 总被引:5,自引:2,他引:5
目的 观察扇贝提取物 (SE)对肝损伤小鼠抗氧化功能的影响。方法 一次灌胃6% CCl4 油溶液 1 0 ml/kg bw,通过谷胱甘肽过氧化物酶 (GSH- Px)、超氧化物歧化酶 (SOD)、脂质过氧化物 (LPO)等指标观察给予 0 .5、1 .5、3.0 (g/kg)扇贝提取物的作用。结果 给予不同剂量扇贝提取物降低 LPO、提高 GSH- Px及 SOD的作用不同 ,以 1 .5g/kg bw效果最好。结论 扇贝提取物可能具有保护肝脏的作用 相似文献
18.
Dimethylnitrosamine (N-nitrosodimethyamine) is a potent inducer of microsomal lipid peroxidation in the liver and kidneys. The results of this study show that prior exposure of adult rats to cadmium or zinc antagonises the effect of dimethylnitrosamine on lipid peroxidation by inducing increased metallothionein synthesis. Increased concentration of reduced glutathione (GSH) in the liver and kidney of rats pre-treated with cadmium or zinc and exposed to dimethylnitrosamine suggests that metallothionein inhibits oxidative stress. The presented results have been corroborated by findings that exposure of adult rats to cadmium or zinc may activate genes for metallothionein and glutathione-S-transferase, the protective proteins against oxidative stress. 相似文献
19.
烟叶硒蛋白在实验性小鼠肝损伤中的抗氧化作用 总被引:12,自引:0,他引:12
观察了烟叶硒蛋白(Se-Rubisco)对四氯化碳肝损伤小鼠的保护作用。结果表明了一次灌胃6%四氯化碳油溶液10ml/kgbw可使小鼠肝组织严重受损,谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活力急剧降低,脂质过氧化产物丙二醛(MDA)显著上升。若提前补充烟叶硒蛋白或亚硒酸钠7d,则可降低CCl_4对肝的损伤,并呈现出剂量效应关系,同时在抗脂质过氧化方面,硒蛋白明显优于亚硒酸钠和不含硒蛋白(Rubisco)组。 相似文献
20.
Benzene is a frequently used industrial solvent. Its toxic manifestations could be modified by sex hormones, but mechanisms of their action are poorly understood. We have examined the influence of progesterone on lipid peroxidation (malondialdehyde), reduced glutathione (GSH), and cytochrome P450 2E1 (CYP2E1) in the liver and kidneys of female rats. Progesterone applied to benzene-treated rats inhibited the formation of reactive oxygen species (ROS), but in ovariectomised benzene-treated rats it significantly increased GSH in the liver. No improvement in CYP2E1 activity was observed in progesterone treated rats. Our results evidence that progesterone changes benzene toxicity (generation of ROS, oxidative stress). However, the probable antioxidative effect of progesterone needs to be confirmed by further studies. 相似文献